哈卡特
CXCL10型
活力测定
STAT1
分子生物学
免疫印迹
化学
MTT法
磷酸化
细胞
体外
趋化因子
生物
生物化学
受体
基因
作者
Manyuan Xu,Zhongsheng Min,Yuegang Wei
出处
期刊:PubMed
日期:2018-08-01
卷期号:34 (8): 708-713
被引量:1
摘要
Objective To detect the effect of glycyrrhizin (GL) on the expression of CXCL10 induced by IFN-γ in HaCaT cells. Methods HaCaT cells were cultured in vitro. IFN-γ at the dosage of 10 ng/mL was used to establish the model group. GL (0.5 mmol/L), JAK1/2 inhibitor CYT387 (15 nmol/L), and combined therapy of GL and CYT387 were administrated in IFN-γ-treated HaCaT cells, respectively. Cell viability was detected by MTT assay. The expression of CXCL10 was assessed via real-time quantitative PCR and ELISA. Protein phosphorylation of the JAK1/2 and STAT1 was determined using western blot analysis. Results GL decreased IFN-γ-induced keratinocyte disruption. Moreover, GL had no significant effect on cell viability. Both GL and JAK1/2 inhibitor CYT387 down-regulated the expression of CXCL10 in HaCaT cells induced by IFN-γ. Its expression of CXCL10 mRNA was markedly lower in GL and CYT387 combined with GL group than that in CYT387 group. The phosphorylation of JAK1/2 and STAT1 declined by GL. Conclusion GL inhibits the activation of IFN-γ- mediated JAK/STAT1 signaling, thereby reducing CXCL10 level in HaCaT cells.
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